Abstract: Chronic deficits in auditory communication following early life seizures Early life seizures (ELS) are prevalent and affect approximately 3/1000 infants. Many individuals with social and communicative deficits, have a history of ELS. ELS and epilepsy correlate with deficits in auditory communication. Initial experimental evidence suggests that ELS cause chronic abnormalities in social behavior and result in vocalization deficits. This leads to the question, if present, what is the nature of auditory communicative deficits triggered by ELS? This must first be addressed in order to understand how these deficits may or may not contribute to the manifestation of chronic social abnormalities following ELS. Clinically the influence of ELS on causation and severity of social deficits remains correlative. An animal model is required to clarify causation and identify underlying mechanisms. Gaps in knowledge: 1. Communication has not been thoroughly explored in any ELS model and the need to complete this assessment has been highlighted. 2. Auditory communicative deficits associated with developmental disorders are not well understood. It is unknown if abnormal auditory function contributes to social deficits seen following ELS. The proposed studies are a first step towards answering this question. 3. A behavioral testing paradigm to thoroughly assess auditory communicative deficits associated with neurodevelopmental disorders is lacking. Goals: We will develop a behavioral test battery to assess auditory communication in rodent models of neurodevelopmental disorders. We will explore deficits in communication following ELS and determine if these deficits impact receptive and/or expressive auditory communication. Supported by preliminary data, we hypothesize that ELS results in chronic socially relevant auditory communicative deficits. These communicative abnormalities may contribute to social deficits in this model and these findings may be applicable to neurodevelopmental disorders that manifest social/communicative abnormalities. Our research will allow future work to explore the underlying mechanistic changes with the aim of rescuing the chronic phenotype. We will assess the ability to respond to and express socially relevant auditory cues in a rat model of ELS with the following specific aims: Expected outcomes: We will determine if socially relevant auditory processing deficits exist in a clinically relevant ELS model. By comparing these results with olfactory communicative function, we will determine if communicative deficits are restricted to auditory communication, suggesting that auditory communicative deficits that occur following ELS contribute to social abnormalities. Alternatively, communicative deficits may extend to the olfactory modality, suggesting that deficits may be the result of reduced social motivation. Our studies may suggest that targeting auditory processing deficits is a viable strategy to rescue deficits associated with ELS, including social deficits. Results may also indicate that aggressive treatment of ELS may prevent the development of chronic communicative deficits.